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Summary

Epidemiological Evidence* The epidemiological evidence pertaining
to the relationship between selenium and cancer is derived from a limited
number of geographical correlation studies in which the risk of cancer
was correlated with estimates of per capita selenium intake, with the
selenium levels in blood specimens, or with selenium concentrations in
water supplies. Although these studies generally demonstrated an in-
verse relationship between the level of selenium and the risk of cancer,
it is not clear whether this relationship applies to all cancer sites or
only to specific cancer sites, such as those in the gastrointestinal
tract. There are as yet no data from case-control or cohort studies.

Experimental Studies. Numerous experiments in animals have demon-
strated an antitumorigenic effect of selenium. The relevance of most
of these studies to the risk of cancer for humans is not apparent since
the levels of selenium used far exceeded dietary requirements and often
bordered on levels that might be toxic. However, one experiment has
demonstrated increased susceptibility to DMBA-induced tumors when se-
lenium deficiency was aggravated by high dietary levels of polyunsatu-
rated fatty acids, and protection by a physiological supplement of se-
lenium (0.1 yg/g) to the diet (Ip and Sinha, 1981). The interpretation
of these results is further complicated because of the varied protocols
used in these experiments and the knowledge that selenium interacts with
many other nutrients, such as heavy metals in the diet.

The minimum requirement for selenium in mammalian species is 0.05
yg/g of diet, one-hundredth of the levels used in many studies of car-
cinogenesis. A level of 4 or 5 yg/g may not be acutely or even chroni-
cally toxic when fed along with a well-balanced, nutritious diet, but it
becomes chronically toxic when the quality of the diet is lowered, for
example when the protein content is reduced. At least two experiments
have demonstrated that selenium deficiency enhances carcinogenesis and
that physiological amounts of selenium have a significant protective
effect. The effectiveness of doses in the wide range between the
nutritionally adequate and the higher, effective level used in many
antitumorigenic studies has not yet been adequately Investigated. The
data on the mutagenicity of selenium compounds are also contradictory.
However, these experiments provide sufficient evidence to suggest that
the antitumorigenic effect of selenium should be investigated further.
Recent data do not support the earlier reports that selenium per se is
carcinogenic.

Conclusion

Both the epidemiological and laboratory studies suggest that
selenium may offer some protection against the risk of cancer. However,
firm conclusions cannot be drawn on the basis of the present limited
evidence. Increasing the Selenium intake to ffiore than 200 yg/day (the